You like our title? Because that's basically the information we're about to give you. This study, which was likely from the Phase II trials of Jan '03 but just posted today in PubMed, shows unquestionable efficacy for Antegren (natalizumab) in a novel measure: Preventing the worsening of new lesions. Note this: The study presumes that Antegren reduces the number of new lesions-- it is exploring what happens to the lesions that DO form when a patient is on Antegren.
Basically this means two things:
1) Antegren reduces lesions
2) When lesions do appear, they do not get as severe (in size/activity) as they would if not on treatment
No word on side effects or long term stability, but containing our enthusiasm for this new treatment which has multi-modal effects (especially compared to the limited efficacy of the CRABs), becomes harder with every story we publish. Let's hope no hidden secrets are going to come up and ruin our fun...but enough of the conservatism; read and enjoy-- a new ray of hope is around the corner. As previous stories have mentioned, Antegren is up for fast-track FDA approval and *may* be available by the end of this year or early next if the FDA permits.
"BACKGROUND: Natalizumab, a humanized monoclonal anti-adhesion molecule antibody, reduces the frequency of new gadolinium (Gd) enhancing lesions and relapses in multiple sclerosis (MS). Its effect on evolution of new Gd enhancing lesions to T1 hypointense lesions is unknown.
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CONCLUSION: Natalizumab significantly suppresses the evolution of new Gd enhancing to T1-hypointense lesions. This may reflect several mechanisms including reduced cell migration across the blood brain barrier, reduced T cell activation within lesions, an inhibitory effect on subsequent axonal damage within the new central nervous system lesion, and a reduced likelihood of recurrent lesion inflammation."
Please click "read more" to get the full abstract...
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Full Article Text
Effect of natalizumab on conversion of gadolinium enhancing lesions to T1 hypointense lesions in relapsing multiple sclerosis.
Dalton CM, Miszkiel KA, Barker GJ, MacManus DG, Pepple TI, Panzara M, Yang M, Hulme A, O'Connor P, Miller DH.
Institute of Neurology, London, UK.
BACKGROUND: Natalizumab, a humanized monoclonal anti-adhesion molecule antibody, reduces the frequency of new gadolinium (Gd) enhancing lesions and relapses in multiple sclerosis (MS). Its effect on evolution of new Gd enhancing lesions to T1 hypointense lesions is unknown. METHODS: 213 patients were randomized to receive 3 mg/kg or 6 mg/kg natalizumab or placebo monthly for 6 months and then followed for a further 6 months. A subset of patients who had one or more new gadolinium enhancing lesions from Month 0 to Month 6 and available electronic data were analysed. Each new Gd enhancing lesion that developed during treatment (months 1-6) was investigated for conversion to a new T1 hypointense lesion at month 12. Lesions were classified as large or small if their cross-sectional area was greater or less than 20mm(2). Because of the similarity of both doses of natalizumab on the frequency of new Gd enhancing lesions, the two natalizumab arms were combined in all analyses. RESULTS: Compared with the placebo group, the natalizumab group exhibited significant decreases in: (i) the proportion of patients with new Gd enhancing lesions that evolved to T1-hypointense lesions (10/38 [26 %] versus 27/40 [68 %]; p < 0.01); (ii) the proportion of patients who developed large T1 hypointense lesions (2/38 [5 %] versus 16/40 [40 %]; p < 0.01); (iii) the proportion of new Gd enhancing lesions that became T1 hypointense (11/75 [15 %] versus 118/466 [25 %]; p = 0.045); (iv) the mean proportion per patient of new Gd enhancing lesions that converted to T1-hypointense lesions (0.15 versus 0.28; p = 0.005), and (v) the odds ratio (OR) of converting from Gd enhancing to T1-hypointense lesions (OR = 0.48; 95% CI = 0.24, 0.94, p = 0.031)). CONCLUSION: Natalizumab significantly suppresses the evolution of new Gd enhancing to T1-hypointense lesions. This may reflect several mechanisms including reduced cell migration across the blood brain barrier, reduced T cell activation within lesions, an inhibitory effect on subsequent axonal damage within the new central nervous system lesion, and a reduced likelihood of recurrent lesion inflammation.
Original article can be found here
